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This Article Full Text Full Text (PDF) Supplementary Reference List All Versions of this Article: 93/6/725    most recent expphysiol.2007.041814v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Kasparov, S. Articles by Teschemacher, A. G. PubMed PubMed Citation Articles by Kasparov, S. Articles by Teschemacher, A. G. Related Collections Cardiovascular control Review Articles

¹ Department of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, UK

Numerous studies, some of which date back more than three decades, have established a link between disorders of the cardiovascular system and the catecholaminergic system of the brain. Central noradrenergic (and putative adrenergic) neurones are involved in numerous brain functions, and there appears to be more than one mechanism via which a dysfunction of central nor/adrenergic signalling may be detrimental to the cardiovascular system. Moreover, in some cases, such as essential hypertension, altered noradrenergic transmission could play a causative role. Numerous controversies are evident throughout the literature, which are very difficult to explain without much better understanding of the basic physiology of central noradrenergic transmission. Recently, using a combination of novel molecular, electrochemical and imaging techniques, we have started to unravel how noradrenergic neurones in the brain store and release their transmitter. Targeted long-term modulation of specific noradrenergic cell groups in defined brain areas using viral gene transfer is helping to clarify the links between central catecholamines and cardiovascular control in health and disease. These studies may reveal new therapeutic strategies for various cardiovascular diseases which are accompanied by heightened sympathetic nerve activity.

(Received 18 December 2007; accepted after revision 29 February 2008; first published online 7 March 2008)
Corresponding author A. G. Teschemacher: Department of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, UK. Email: Anja.Teschemacher{at}bristol.ac.uk